Study on behavioral characteristics of wild and hatchery-reared red tilefish

Organized by Graduate School of Informatics, Kyoto University ; JSPS Bangkok Liaison Office ; Japanese Society of Bio-logging Science ; Informatics Research Center for Development of Knowledge Society InfrastructureDecember 13-15, 2004, Imperial Tara Hotel, Bangkok, ThailandThe diel activity of red tilefish Branchiostegus japonicus was studied using two different methods : analysis of biotelemetry records and video observation. We have acquired the biotelemetry tracking records of the red tilefish which were released in Maizuru Bay and tracked from January 2003 to February 2004. The records ware compared to the time of sunrise and sunset, the duration of sunshine, and the lunar cycle, which may influence on light conditions. Whilst the fish showed diel activity, the fish changed their behaviors along with the time of sunrise and sunset; the fish probably moved out of their burrows in the daytime and retreated into the burrows at night. We could not find a clear relationship between the behavior and the other two factors. In the laboratory, the behavior of one hatchery-reared individual was recorded by video for five days in the experimental tank where the light condition changed periodically over 24 hours. The fish was more active in the light periods (550 lx) compared to in the dark periods (0 lx). Since the results from the two methods probably compliment one another, further experiments using the two methods will reveal the detailed behavior of red tilefish

X-ray structure of Galdieria Rubisco complexed with one sulfate ion per active site

AbstractRibulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco) catalyzes the reactions of carboxylation and oxygenation of ribulose-1,5-bisphosphate. These reactions require that the active site should be closed by a flexible loop (loop 6) of the large subunit. Rubisco from a red alga, Galdieria partita, has the highest specificity for carboxylation reaction among the Rubiscos hitherto reported. The crystal structure of unactivated Galdieria Rubisco has been determined at 2.6 Å resolution. The electron density map reveals that a sulfate binds only to the P1 anion-binding site of the active site and the loop 6 is closed. Galdieria Rubisco has a unique hydrogen bond between the main chain oxygen of Val332 on the loop 6 and the ϵ-amino group of Gln386 of the same large subunit. This interaction is likely to be crucial to understanding for stabilizing the loop 6 in the closed state and to making a higher affinity for anionic ligands

p53 family network and human cancer

Since the 1980s cancer is the leading cause of death in Japan. Most human cancers exhibit inactivation of the p53 network, either through direct mutation of p53,or through disruption of regulatory pathways essential for p53 function.The tumor suppressor gene p53 encodes a transcriptional activator as a nodal point for cellular responses to several stress conditions. p53 is one of the most highly connected nodes in the cell,and an attack on p53 by mutation will disrupt basic cellular functions, particularly responses to DNA damage and tumor-predisposing stresses. p63 and p73 are functionally and structurally related to the tumor suppressor p53. Recent findings from others and us have provided evidence for a broader role for the p53 family than were previously reported. In this review, we provide an overview of the networks controlled by the p53 family as a framework for developing p53 family-based strategies to treat cancer

Tim23–Tim50 pair coordinates functions of translocators and motor proteins in mitochondrial protein import

Mitochondrial protein traffic requires coordinated operation of protein translocator complexes in the mitochondrial membrane. The TIM23 complex translocates and inserts proteins into the mitochondrial inner membrane. Here we analyze the intermembrane space (IMS) domains of Tim23 and Tim50, which are essential subunits of the TIM23 complex, in these functions. We find that interactions of Tim23 and Tim50 in the IMS facilitate transfer of precursor proteins from the TOM40 complex, a general protein translocator in the outer membrane, to the TIM23 complex. Tim23–Tim50 interactions also facilitate a late step of protein translocation across the inner membrane by promoting motor functions of mitochondrial Hsp70 in the matrix. Therefore, the Tim23–Tim50 pair coordinates the actions of the TOM40 and TIM23 complexes together with motor proteins for mitochondrial protein import

Pace running of a quadruped robot driven by pneumatic muscle actuators : An experimental study

Our goal is to design a neuromorphic locomotion controller for a prospective bioinspired quadruped robot driven by artificial muscle actuators. In this paper, we focus on achieving a running gait called a pace, in which the ipsilateral pairs of legs move in phase, while the two pairs together move out of phase, by a quadruped robot with realistic legs driven by pneumatic muscle actuators. The robot is controlled by weakly coupled two-level central pattern generators to generate a pace gait with leg loading feedback. Each leg is moved through four sequential phases like an animal, i.e., touch-down, stance, lift-off, and swing phases. We find that leg loading feedback to the central pattern generator can contribute to stabilizing pace running with an appropriate cycle autonomously determined by synchronizing each leg’s oscillation with the roll body oscillation without a human specifying the cycle. The experimental results conclude that our proposed neuromorphic controller is beneficial for achieving pace running by a muscle-driven quadruped robot

Significance of Coronary Artery Calcium Score in the Target Lesion Evaluated by Multi-detector Computed Tomography for Selecting Treatment of Rotational Atherectomy in Patients with Coronary Artery Disease

We investigated whether coronary artery calcium score (CAC) in the target lesion on the multidetector computed tomography angiography (CTA) predicts the addition of the Rotational atherectomy (Rota) during percutaneous coronary intervention (PCI). Lesion CAC on CTA were evaluated with quantitative coronary analysis (QCA) on coronary angiography for predicting the Rota treatment in 114 consecutive patients (165 target lesions) with first PCI (68 ± 9 years old, females: 17.6%). Rota was added in 8 patients (11 lesions). The lesion length and diameter stenosis on QCA, and lesion length and lesion CAC on CTA were the primary factors associated with the addition of Rota. Using the cut-off value based on receiver operating characteristic analysis, the sensitivity and specificity for predicting the Rota based on QCA was 72.7% in 8 of 11 lesions (vessels) with Rota and the specificity was 74% in 114 of 154 without Rota in the lesion length of ≥ 23mm (χ2=10.9, p=0.001), and 54.5% in 6 of 11 lesions with Rota and the specificity was 79.2% in 122 of 154 without Rota in the diameter stenosis of ≥ 83% (χ2=6.6, p=0.01). Those based on CTA were 90.9% in 10 of 11 lesions with Rota and 77.3% in 119 of 154 without Rota in the lesion length of ≥ 34mm (χ2=24.1, p<0.001), and 90.9% in 10 of 11 with Rota and 88.3% in 136 of 154 without Rota in the lesions with CAC ≥453 (χ2=45.7, p<0.001). Lesion CAC on CTA is most predictive of addition of Rota during PCI

Significant association of RNF213 p.R4810K, a moyamoya susceptibility variant, with coronary artery disease

Background The genetic architecture of coronary artery disease has not been fully elucidated, especially in Asian countries. Moyamoya disease is a progressive cerebrovascular disease that is reported to be complicated by coronary artery disease. Because most Japanese patients with moyamoya disease carry the p.R4810K variant of the ring finger 213 gene (RNF213), this may also be a risk factor for coronary artery disease; however, this possibility has never been tested. Methods and results We genotyped the RNF213 p.R4810K variant in 956 coronary artery disease patients and 716 controls and tested the association between p.R4810K and coronary artery disease. We also validated the association in an independent population of 311 coronary artery disease patients and 494 controls. In the replication study, the p.R4810K genotypes were imputed from genome-wide genotyping data based on the 1000 Genomes Project. We used multivariate logistic regression analyses to adjust for well-known risk factors such as dyslipidemia and smoking habits. In the primary study population, the frequency of the minor variant allele was significantly higher in patients with coronary artery disease than in controls (2.04% vs. 0.98%), with an odds ratio of 2.11 (p = 0.017). Under a dominant model, after adjustment for risk factors, the association remained significant, with an odds ratio of 2.90 (95% confidence interval: 1.37-6.61; p = 0.005). In the replication study, the association was significant after adjustment for age and sex (odds ratio = 4.99; 95% confidence interval: 1.16-21.53; p = 0.031), although it did not reach statistical significance when further adjusted for risk factors (odds ratio = 3.82; 95% confidence interval: 0.87-16.77; p = 0.076). Conclusions The RNF213 p.R4810K variant appears to be significantly associated with coronary artery disease in the Japanese population

TRAF6 Establishes Innate Immune Responses by Activating NF-κB and IRF7 upon Sensing Cytosolic Viral RNA and DNA

BACKGROUND:In response to viral infection, the innate immune system recognizes viral nucleic acids and then induces production of proinflammatory cytokines and type I interferons (IFNs). Toll-like receptor 7 (TLR7) and TLR9 detect viral RNA and DNA, respectively, in endosomal compartments, leading to the activation of nuclear factor kappaB (NF-kappaB) and IFN regulatory factors (IRFs) in plasmacytoid dendritic cells. During such TLR signaling, TNF receptor-associated factor 6 (TRAF6) is essential for the activation of NF-kappaB and the production of type I IFN. In contrast, RIG-like helicases (RLHs), cytosolic RNA sensors, are indispensable for antiviral responses in conventional dendritic cells, macrophages, and fibroblasts. However, the contribution of TRAF6 to the detection of cytosolic viral nucleic acids has been controversial, and the involvement of TRAF6 in IRF activation has not been adequately addressed. PRINCIPAL FINDINGS:Here we first show that TRAF6 plays a critical role in RLH signaling. The absence of TRAF6 resulted in enhanced viral replication and a significant reduction in the production of IL-6 and type I IFNs after infection with RNA virus. Activation of NF-kappaB and IRF7, but not that of IRF3, was significantly impaired during RLH signaling in the absence of TRAF6. TGFbeta-activated kinase 1 (TAK1) and MEKK3, whose activation by TRAF6 during TLR signaling is involved in NF-kappaB activation, were not essential for RLH-mediated NF-kappaB activation. We also demonstrate that TRAF6-deficiency impaired cytosolic DNA-induced antiviral responses, and this impairment was due to defective activation of NF-kappaB and IRF7. CONCLUSIONS/SIGNIFICANCE:Thus, TRAF6 mediates antiviral responses triggered by cytosolic viral DNA and RNA in a way that differs from that associated with TLR signaling. Given its essential role in signaling by various receptors involved in the acquired immune system, TRAF6 represents a key molecule in innate and antigen-specific immune responses against viral infection

Comprehensive genomic profiles of small cell lung cancer

We have sequenced the genomes of 110 small cell lung cancers (SCLC), one of the deadliest human cancers. In nearly all the tumours analysed we found bi-allelic inactivation of TP53 and RB1, sometimes by complex genomic rearrangements. Two tumours with wild-type RB1 had evidence of chromothripsis leading to overexpression of cyclin D1 (encoded by the CCND1 gene), revealing an alternative mechanism of Rb1 deregulation. Thus, loss of the tumour suppressors TP53 and RB1 is obligatory in SCLC. We discovered somatic genomic rearrangements of TP73 that create an oncogenic version of this gene, TP73Dex2/3. In rare cases, SCLC tumours exhibited kinase gene mutations, providing a possible therapeutic opportunity for individual patients. Finally, we observed inactivating mutations in NOTCH family genes in 25% of human SCLC. Accordingly, activation of Notch signalling in a pre-clinical SCLC mouse model strikingly reduced the number of tumours and extended the survival of the mutant mice. Furthermore, neuroendocrine gene expression was abrogated by Notch activity in SCLC cells. This first comprehensive study of somatic genome alterations in SCLC uncovers several key biological processes and identifies candidate therapeutic targets in this highly lethal form of cancer